Brain Images Link Strokes to Heart Damage

Action Points

Explain to interested patients that this study found evidence of a relationship between ischemic strokes in the right insula region of the brain and a 15-fold risk of stroke-related myocardial damage. This was not so as a result of strokes in other brain regions.

BOSTON, April 25 - Ischemic strokes in two specific area of the brain appear to send shockwaves through the sympathetic nervous system to cause myocardial injury.

Magnetic resonance imaging studies of patients who had new evidence of myocardial damage following an ischemic stroke indicated that infarctions occurring in the right insula and right inferior parietal lobule regions of the brain might be to blame, researchers here reported in an early online release in Neurology.

"The link between the brain and the heart in stroke patients is fascinating," said A. Gregory Sorensen, M.D., of Massachusetts General Hospital. "For instance, most patients with acute stroke have elevated blood pressure that returns to baseline over three to seven days. The connection is believed to be through the autonomic nervous system, but what the mechanism is has been unclear.

"By finding a specific brain area associated with a dramatically increased risk of heart damage, we can identify at-risk patients when they arrive at the hospital and put them on protective therapy, which should have a direct impact on their care," he continued.

Dr. Sorensen and colleagues at MGH and Harvard Medical School looked at 738 consecutive patients with acute ischemic stroke and identified 50 who had elevated serums levels of cardiac troponin T in the absence of any apparent cardiac cause within three days of the onset of stroke symptoms.

They randomly selected an additional 50 age- and sex-matched patients who had suffered ischemic strokes without apparent myocardial injury as controls.

The groups had similar stroke risk factors, history of coronary artery disease, infarction volume, and frequency of right and left middle cerebral artery territory involvement.

The investigators assembled diffusion-weighted MRI imaging studies taken during initial clinical evaluations of each patient and created outlines of infarctions. They co-registered the images to a template and averaged them to create a detailed brain map. They then used digital subtraction to detect voxels (volume pixels) that differed between the patients with myocardial injury and controls.

"Brain regions that were a priori associated with cardiac troponin T elevation included the right posterior, superior, and medial insula and the right inferior parietal lobule," the authors wrote.

In all, 17 of the patients in the elevated troponin group and 21 of those in the normal troponin group had infarctions in the right middle cerebral artery territory. Among these patients, the insular cluster was involved in 88% of those with evidence of myocardial damage, compared with 33% of those without marker elevation. The odds ratio for heart damage from a stroke in the right insular area was 15.00 (95% confidence interval 2.65 to 84.79).

The authors noted that the insula is the site for integration of sensory, autonomic, and limbic functions, and that studies in animal models have linked the region to cardiac autonomic control.

"We speculate that an infarction in the right posterior insula might cause disinhibition of other centers, such as more anterior insular sites, that in turn leads to enhanced cardiac sympathetic activity and related myocardial injury," they wrote.

They acknowledged, however, that they could not explain the link between myocardial injury and strokes in the right inferior parietal lobule. This region, which shares an arterial supply with the right insula, could be a "bystander," the authors speculated.

"In treating stroke patients, we often raise their blood pressures to try and increase blood flow into the affected areas, but we don't know why that works well for some patients and not for others," said Walter Koroshetz, M.D., a co-author. He is director of the MGH Stroke and Neurointensive Care Service.

"This technique may help us identify which patients will do well with that approach, and it has great potential for helping us get unbiased answers to many other questions regarding localized effects in the brain," Dr. Koroshetz added.

The authors pointed out that "despite the stringent criteria to exclude patients with acute coronary syndromes, in some of our patients, troponin T elevation might have been caused by exacerbation of coincident coronary artery disease. There is currently no available test to be used for such distinction."

However, they wrote that "our data imply that there might be a troponin T threshold that differentiates between neural and cardiac mechanisms of troponin T elevation; most troponin T elevations in the current study were modest, not exceeding 1 ng/mL in 96% of the patients. In contrast, troponin T levels typically increase up to 50 times of the upper reference limit when measured 18 to 24 hours after an acute coronary syndrome."

Reviewed by Zalman S. Agus, MD Emeritus Professor at the University of Pennsylvania School of Medicine